• LecturehallThe Complex Cavus Foot: Common Presentations and Surgical Corrective Options
  • Lecture Transcript
  • TAPE STARTS – [00:00]

    Speaker: Coming up next to the podium we are going to hear from Dr. Andrew Belis. He is going to be talking to us about the complex cavus foot. Dr. Belis was born and raised in Long Island, New York, received his bachelor’s degree in human physiology at Boston University prior to attending Temple Podiatric Medical School. He completed his first residency at WycKoff Heights Medical Center in Brooklyn. His second residency program is at the Greater Baltimore Medical Center in Maryland, which is near and dear to my heart. Dr. Belis is an associate faculty member at Florida State University Family Medicine Residency Program. He serves on the board of directors for the American Society of Podiatric Surgeons and is an executive board of the Florida Podiatric Medical Association and is currently the president. He is a fellow of the American College of Foot and Ankle Surgeons and is double board certified American Board of Foot and Ankle surgeon. Dr. Belis came today from Cape Coral in Fort Myers area in 2002 with his wife and he has three wonderful children. So please give him a warm welcome for Dr. Andrew Belis.

    Dr. Andrew Belis: Okay. Thank you for having me. So I hated the cavus foot going through school and because there is a huge component of neurology involved with this, so that was always my nemesis. So I have learned to master it and really embraced it because it does become a big part of my practice. And I think you will see it becomes a big part of your practice as well. And these things don't just jump out. You really have to screen people for it and you have to be aware of it and start looking for it as well. So today we are going to be going over the etiology, diagnosis, decision making algorithms that I use, conservative options as well as surgical options for management.


    As mentioned, I am a consultant for Arthrex and Bioventus, but they do not apply to this lecture. So cavus foot, we all know what that is, it is a high-arch foot, fails to flatten out or pronate during gait or standing. So this has been studied over time since the 1880s and basically different surgeons and physicians have observed the different patterns and come up with different solutions over time. What I would like to talk about is this article or this bulletin in 1963. He came up with this retrospective review that cavus foot type, 81% of it was idiopathic. So you know idiopathic means we don’t know what the heck is going on here. So he started a cavus clinic where he actually -- it was an orthopedist and neurologist, and they reviewed these cases, these patients and they came up with 77 patients and out of those, 66% of them had an obvious neurologic disorder, 34% then were classified as idiopathic. Now from those, he went back and did additional studies and showed that 27% of those 34% actually ended up having neurogenic deformities here. So this is something you want to really look for and screen and really have a good relationship with your neurologist or physiatrist that do these EMG studies. In 1977, Coleman came up with this simple technique and I think we should all these in your office and if you don't do this, get a piece of block and do this in your office just to determine if the cavus is coming from the rear foot or not, the fixed versus the flexible hind foot, and this is just the simplest thing that you can analyze in your office. So if the rear foot is fixed and in inverted position, it will not neutralize or evert when you offload the forefoot, the submet 1 to the ground. So basically you are putting the heel on the edge of a block and allowing the first ray to fall and if your heel does not change, then it is a fixed rear foot cavus. This is very important concept because this will help you determine if you can actually brace these people and what type of surgical intervention you are going to need here.


    So again 60% of all cavus feet will develop some pain. I think this is a more prevalent painful problem than a flat foot. And flat foot gets all the attention but cavus feet really -- there is significant problems here, 10% prevalence population. So there are different origins for the cavus foot type and neurogenic contributions to a cavus. There is brain, spinal cord, peripheral nerves, trauma, bone and then there is that idiopathic, which we will hate because we don't know what the heck is going on there. Brain tumor, CP stroke, spinal cord, you have your tumors, polio, spinal dysraphism, CMT, this is a really common one that we see and I think you will all see as well. And then there are traumatic nerve injuries as well. Trauma and there is coalition and malunion situation as well. So neurogenic, the CMT, Friedreich ataxia, CP, we have talked about that. So the most common one that I see is CMT, 10 to 30% out of 100,000. It is a group of inheritable defect. So there are different types, subtypes and it is inheritable. You have mild degeneration and axonal degeneration here. So it is a progressive problem. It is lower motor neuron. It is not spastic but there is antagonist- agonist imbalance. And really by the way, there is going to be a test later, so you want to remember this part. There is intrinsic muscle wasting, which happens first and you get your digital contractures. It is usually rigid. Then you have peroneal brevis weakness where the longest is spared. And this is really important because you will see this affect the forefoot as it relates to rear foot. I think you have your tibialis anterior where EHL is spared. So again you get these classic deformities here. I am going to skip through that one.


    So CP is also common. This is a permanent static lesion usually occurs in the cerebral motor cortex. It occurs before two years or at two years or at birth. The lesion is nonprogressive. It is a static lesion. So basically presentation stays the same but deterioration could occur from other reasons. There is CNS hemorrhagic, mechanical spinal cord or brainstem damage can occur and again it is a deep CNS hypoxic. Okay. So you can have different types of classifications for CP. You have your spastic, which is the majority, 70% to 80%. You have your diskinesic less than 25% and you have ataxic, which is 10%. So just watching these people walk, you will get a feel for which type they are falling into and you could see which part of their brain is being affected accordingly. There is spinal dysraphism as well. These are congenital deformities, definitely it's a neurogenic component and you can have traction on the spinal cord, tethered cord syndrome. So then there is polio. That’s an infectious disease. It is an enterovirus. It is a fecal oral route. Anterior horn cells of the spinal cord are affected here. It is a lower motor neuron disease. It is most likely to affect young children and usually happens in communities, bathing in underdeveloped countries where there is that fecal oral route transfer. Again, we did a good job trying to eliminate this. Back in 2016, three countries still had polio, were still endemic and less than 40 children were paralyzed as a result of this. So 90% that are infected are asymptomatic and only 10% are symptomatic, which is good, I guess. Categories, there is minor, which is abortive and severe. Non-paralytic where you can get aseptic meningitis, paralytic and the classic deformities of hind foot cavus.


    And this is really important to remember this part. Your gastrocsoleus complex is weak in polio patients and that's important at least to calcaneus alignment of your heel and the long flexor tendons are plantar flexing with a little bit more strength, so you are getting this forefoot cavus and rear foot cavus and that's important because that will affect if you need to fix these patients or treat these patients where you are going to be looking for. Traumatic injuries can occur. CVAs, traumatic brain injuries, spinal injuries, those types of things. CVAs, this is one of the primary causes of hemiplegia, third leading cause of death in United States, ischemic versus hemorrhagic. And again a lot of us see this, especially down in Florida, we see a lot of CVA patients, post CVA. Understanding this also helps you identify you know at what stage you are going to treat these patients in because these patients can rebound a little bit and there is different timeframes, I will talk about that as far as when you want to intervene if you want to intervene. You get acute flaccid paralysis with CVAs, post stroke, hypertonia up to 70%. The deforming forces are the foot or the tibialis anterior and triceps and you can have equinovarus deformity at least to a painful limitation of gait. So this is an important slide as well because you can see that sometimes recovery happens up until six months. So you may not want to start operating on these patients right away for weakness. Bracing them in the beginning stages is really important. Letting them go through their physical therapy, letting them try to rebound, that is really important part of this technique that you are going to treat. If they end up having problems after the six-month mark, then you can consider intervening at this point with more surgical intervention. Traumatic brain injuries, this is usually in the younger population. It is usually direct blow, trauma, work injuries, car accidents and there is variable recovery with these, two to four years.


    Again different reasons for spinal injuries, that's another cause of neurogenic component here. Motor vehicles, most common we see, accidents of workman's comp patients, falls, different types of sporting activities. Okay. So we go through that, the various components of the types of cavus because not all cavus feet are the same. You have that hind foot cavus that we talked about with polio, forefoot cavus we talked about with CMT. We can get combined cavus foot type. Definitely MTP deformities and then you have your soft tissue deformities that go with these and don't forget your soft tissue as well because that's really important. Hind foot cavus, again we talked about that, common with polio. You get your chronic ankle sprains, forefoot cavus, plantar flexion have forefoot, again CMT. Biomechanics, so forefoot cavus or the biomechanics is usually driven by the first ray. Peroneal longus over powers the tibialis anterior. You get first ray plantar flexion. Your rear foot supinates to compensate. You get blocking of your MT joint, mid tarsal joint and then that really makes the foot very rigid and very difficult to shock absorb and that can cause some significant pain and clinical symptoms. You get tripod effect. That's how I tell patients. MTP joint deformity, we talked about that. That's usually extensor substitution, retrograde buckling, and you get your forefoot symptoms here. So plantar fascia, this is an interesting concept, which I think with cavus feet very frequently becomes very tight and very sore. Sometimes we do get plantar fasciitis in people with cavus foot type and this is one of the very rare situations where we actually release the plantar fascia. I don't do that anymore for standard plantar fasciitis in a pronating foot. I think it accelerates the pronation. So if you can get to avoid that, that's preferable and usually I do more of the gastroc lengthening for those types of procedures.


    Moving on, we have our clinical history, we talked about that. I want to skip ahead a little bit if you don't mind. Again, hind foot, I look at this as compartmentalizing hind foot, claw toes, muscle strength, stability and types of cavus. If you can identify, then you can identify what's going on here. And don't forget, we talked that these are significantly caused from neurogenic problems. Make sure you get your EMG and CV studies and work with neurology or your physiatrist on management of the underlying disease. Overall, appearance of CMT, you get this stork like appearance, inverted champagne bottle. This is another clinical sign. I look for peek-a-boo sign. When you are looking to the patient straight on, you see their heel inverted. Remember your upper motor neuron problems versus your lower. Lower, you're going to get hyporeflexia, flaccid, Babinski's absent and muscle atrophy. Uppers, you're going to get spasticity, Babinski's present and no muscle atrophy. Again, there is your Babinski, we know how to do that. Look at the hands too. Look for atrophy and weakness. That’s asymmetric or symmetric. There is Coleman block test. I will skip ahead because we have a little more to go through. Deformities, again look for your equinus, look for hind foot varus and these are the different muscles that are going to be antagonizing and agonizing against these types of deformities here. We kind of review that already. Look at imaging and diagnosis. This is really important. So I am going to tell you lot about what's going on here. We look for Meary's angle as far as collapse here in first ray. First ray is really important when you are analyzing a cavus foot type. We talked about that with CMT. With a cavus, you have greater than five degrees normal zero. Calcaneal inclination of ankle is also important for your rear foot cavus. Normal is 18 to 22. Greater than 30, you have that component of rear foot cavus. You have to address that. Radiographic signs that sinus tarsi bullet hole, you aren't getting a true lateral and basically you are having that break of the sym [phonetic] line as well.


    Treatment, so non-operatively we have -- these are rarely successful in progressive disease processes. They can provide for symptomatic relief and they can prolong the need for surgery and sometimes are used with, that we talked about, CVAs and another types of when you are trying to buy yourself sometime to see if the defect can improve. Bracing is, I think we all know this. AFOs, PT, orthotics, what about Botox, what about muscle relaxants, do we use these types of things? Botox is pretty interesting option here to temporarily three months of knocking out of muscle group or nerve function. Cochrane collaborative back in 2010 showed that Botulinum and OTC inserts showed no significant improvement here, but orthotics did. So using orthotics definitely can help buy these patients sometimes, help the deformity and help with the situation. Okay. So surgically what do we do? There are different options and there is no one particular boiler plate option. And again, you have to really thoroughly diagnose these problems to determine, which type of cavus foot type do I've? Is it a progressive problem? Is it spastic? Is it an antagonist or agonist problem? Where is the deformity? Where is the etiology of the issue? So surgical options, so you have several options. The common general principles, number one flexible deformities, you can do soft tissue releases. Rigid deformities, you may need ostetomies or fusions. And to maintain correction, tendon transfer definitely can help here. Late stages with arthritic disease sometimes will require fusions and my threshold for fusions are very low. I feel like with the progressive problems, you may need to do that right off the bed. So again, surgical treatments, hind foot, there is the rigid, there is flexible. So for rigid hind foot problems, you are looking at calcaneal osteotomies, Dwyer, those types of things, shifting osteotomies. For flexible, you may be able to get away with a forefoot procedure if it is driving the rear foot into the flexible deformity.


    Fore foot, you have flexible deformities. Again that's your plantar fasciotomies. Your rigid and mild cavus deformities, you can go with plantar fasciotomy and first MT procedure. Rigid, you are doing all three with mid tarsal osteotomy as well. Toes, we talked about the claw toes. If they are rigid or flexible, tendon transferring or no tendon transferring. Muscle strengths again, you may be looking at tendon transfers or do you augment, you supplement or you release and then for rigid deformities, you know you may have to jump to your triple arthrodesis in skeletally mature bone. Soft tissues, let's go through these real quick. Plantar fascia, you have your Steindler stripping, and then your gastrocnemius lengthening. You also have your MPJ procedures, your tendon transfer zones, Hibbs, splat, peroneal longus, PT tendon transfer. So depending on where the deformity is and where your agonist muscles are, your antagonist muscles, addressing those accordingly. So this is something I think we all forget about using in our armamentarium but this very effective procedure. When you first do these and put patient with cavus foot type, they usually take a while to kind of stretch out and loosen over time, but this is very effective procedure and it is not just the plantar fascia that you are lengthening. You actually have to release the intrinsic muscles as well. Your abductor hallucis, your FDB and your digiti quinti. And really this is just working in the sagittal plane. TALs, Strayer’s, Bowman’s [phonetic], advancements, posterior lengthening, be careful with these. You really want to look at your calcaneal inclination angle and address it accordingly. Again, if you have that polio patient, you are definitely not going to do this. Some of the others, you may have to get your balance there. Even when you are doing these, you really want to be careful that when you do your TALs, you're not over lengthening because you could develop a gait like this -- I mean an x-ray like this.


    Let's move on. We talked about our balancing procedure. I am not going to talk about that too much. Your forefoot tenosuspensions here. These work to help the first ray dorsiflex them, your Hibbs and your tendon transfers depending upon if you have a cavovarus deformity. Post CVA may require these types of procedures. We are transferring the tibialis anterior to the lateral side of the foot decreasing the need for orthotics and improving with function. You have your split tendon transfer, we just talked about that. 35% of these patients were able to discontinue orthotics as a result of this. So these give good results as well. Posterior tibial tendon transfers or even sometimes releases, I have had patients that are very sick. They have a very severe PT tendon strength with weakness to the peroneals. I have done this in my office where we have numb them up and just release the PT tendon and we have had pretty good success with that, especially if you are high-risk really sick patients. Obviously, the better option is to transfer this if you are using it for augmentation for dorsiflexion, but again the PT is a very powerful force in a cavus foot type, so you may want to address this as well. Peroneal brevis to longus. Again, we talked about the peroneal longus being a very strong plantar flexor of the first ray. So if it is causing a flexible plantar flexor deformity that's causing a cavus deformity, sometimes just transferring that to the brevis makes a big difference. It will supplement your brevis and also weaken the peroneal longus, thus improving your alignment. Then we talked about osseous procedures, which really will play a big role in the cavus foot type because some of the soft tissue procedures really don't do enough to make it everything right. Don't forget your dorsiflexion first ray, osteotomy, your Jost’s, Cole’s, Japa’s, Dwyer’s. Arthrodesis really is one of the more aggressive mainstays in my practice and sometimes especially with some of these patients who are endstage, cavus foot type is very rigid.


    Does not have that shock absorption, so these patients usually develop arthritis pretty quickly. So especially in my population in Florida, we see a lot of older people and by the time they come in with us, they really do need some of the more triple procedures. We talked about the rigid plantar flexor first ray and dorsi flexing that. You can either do a first ray osteotomy or even a fusion to correct this deformity. There is just a simple example of a Dwyer plus dorsiflexion first ray and this is a very power procedure and I think in this case we also did a Steindler stripping as well. Again, mid foot, depending on what your apex of your cavus foot type is, you may need to use the different deformities. We talked about the first ray fusion where the first ray dorsiflexion osteotomy. If deformity is little further back in the foot, you can do this mid foot apex type osteotomy, cold type osteotomy to dorsiflex the ray and stabilize the foot. You will have to do a soft tissue procedure with these to augment this in order to get that foot neutralized. There is your osteotomy and then stabilizing it appropriately. Mid foot, we talked about that cold and through the navicular cuneiform joints and the cuboid. Again, different types of osteotomies across the mid foot. We talked about the Japa’s procedure as well and again just depending upon where the deformity is, the first ray may be different than the mid foot and you have to adjust your osteotomy accordingly. We talked about the hind foot cavus and osteotomies and this is also another important thing that I see. Now, you can accomplish correcting a cavus rear foot with either a fusion of subtalar joint and correcting it with removal of the necessary amount of bone versus doing rear foot osteotomy.


    Remember, you want to dorsiflex the posterior tuber and valgus depositioning there to help with that situation. Again, this can also be accomplished with a fusion as well at the subtalar joint. We talked about Dwyer. Remember this is a very -- just like we had mentioned earlier about medializing the calcaneus to improve the cavus pole, the same concept occurs when you are trying to lateralize this. And I will tell you that this procedure isn't done enough in patients and lot of our community or fixing Brostrom and lateral ankle instability. I can tell you I do a lot of second opinions and third opinions and most of the time when the lateral ankle ligament fails, it is because they didn't address the rear foot cavus or rear foot inversion. So using a Dwyer -- my tolerance for Dwyer is very low for patient who has any kind of imbalance of the rear foot or medialization of the rear foot compared to the ankle ligaments in the center of the ankle. So If you have any doubt your lateral ligament repair will fail if you don' correct the rear foot. So really make that part of your learning curve as far as you know adding that procedure. It will add more time and more healing time but again I think it will be worth at long run, so you don't have to fail. We talked about triple arthrodesis as well. This is really the goal standard especially for progressive neurogenic problems. This can maintain your correction and keep everything healed. In my patient population, we also get a lot of obese patients. So doing some of the soft tissues and the osteotomies may not be as effective because of the obesity issue. So what is going to hold up in an obese patient is really going to be a fusion of the rear foot or mid foot depending upon where the deformity is. In addition, one another thing about triple or double and for that matter is that if you have forefoot deformity and if you uncover with your rear foot, you will also have to address your forefoot.


    Too many times, we see either cavus foot or even a flat foot, which obviously we are going to do a triple fix everything. Well, fusion of TN joint is not correct sagittal plane enough for the medial column. So you always want to potentially consent that patient for forefoot procedure as well whether it is a dorsiflexion or plantar flexion first ray or mid foot fusion as well. Again, this is really better for longstanding deformities and these actually have very good success rates especially for these neurogenic based cavus foot type. Long-term studies, again 88% good-to-excellent results. So the literature does support your use of this. I know a lot of us try to avoid fusions. We hear the word fusion. We think patient is never going to walking again. But again, I bring the study just to show that there is really good success rate with these and patients are extremely happy. Remember, a fused foot in a slightly pronated position so much better than a non-fused cavus foot that's still somewhat rigid. So again, my threshold for fusion and triples are very low. As long as you're in the neutral position, the satisfaction rates very pretty high. Okay, so you guys are ready for your test now? So all the following are typical characteristics of an upper motor neuron lesions except, clonus, spasticity, Babinski sign present, muscle atrophy or none of the above. A, B, C, D or E. Come on somebody say something. B? D. You are right. 100% on that one. Okay, what is this test? Right. Let's go back. So this is a patient we are looking at the left picture of the foot and then the right picture is the same.


    Sorry. The left foot is when we are looking at and look at the B and this is the test results that you are seeing. So based on this, given the physical findings what surgical intervention would be the most appropriate? Dwyer with first metatarsal dorsiflexion, triple arthrodesis or first metatarsal dorsiflexion procedure? Before you yell it out, let me look at that one more time. So again, the picture is the left foot and B is also the also the left foot. So Dwyer with first met dorsiflexion, triple or first met dorsiflexion procedure? Okay, now yell it out. B? D? Who says B? Who says D? Excellent. D. So that will be fixed just with that dorsiflexion procedure. Which are the following muscles are typically weak in CMT? EHL, anterior tibial, peroneal longus, peroneal brevis, posterior tibial or intrinsics? For bonus, put them in order. Does anybody want to give us a try come to the microphone? Go ahead, I know you want to.

    Speaker 1: Brevis, intrinsic.

    Dr. Andrew Belis: Brevis and intrinsic? We have one answer for that. Anybody else? Okay. So we have the intrinsics first, so you are right on that one. The peroneal brevis second and the tibialis anterior is the last. Okay. Remember, the peroneal longus over powers the tibialis anterior. The tibialis anterior dorsiflex the first ray, the peroneal longus plantar flexes the first ray. So you guys did great. So thank you very much. I am happy to take any additional questions at this point in time.

    TAPE ENDS - [31:07]